Presentation Authors: Andrew Bosomworth, Pomona, CA, Stephen Freedland, Zhaoxuan Ma, Los Angeles, CA, Jay Fowke, Memphis, TN, Emanuela Taioli, New York, NY, Andre Rogatko, Beatrice Knudsen, Los Angeles, CA, Charles Drake, New York, NY, Adriana Vidal*, Los Angeles, CA
Introduction: Prostate cancer (PC) is the most common non-cutaneous cancer in men and a leading cause of cancer death. In the US, black men are disproportionately affected with higher incidence of and mortality to PC than any other race. We hypothesize that different inflammatory cells may stimulate or inhibit PC development, and that black men have more pro-tumor inflammation contributing to the health disparity seen in PC in the US.
Methods: Prostate biopsies were obtained from 84 men, 50% black/50% white men, with and without PC on biopsy. Using fluorescence microscopy with multiplex immunohistochemistry, biopsy tissue samples were stained for 4 T-cell markers (CD3, CD4, CD8, and FOXP3) and 3 regions were examined (prostate tumor, tumor-free areas surrounding the tumor, and controls or biopsy negative samples). Using T-tests, data were analyzed for type of cell (marker) and cells/mm2 by region. Analyses were stratified by race. An alpha of 0.0125 (after Bonferroni correction p=0.05/4) was used.
Results: Prostate biopsies of black and white men showed several significant differences. Prostate biopsies in black men had statistically significant higher levels of CD8 T-cell expression compared to those of white men (p=8.9x10-8). Black men prostate biopsy tissues displayed higher levels of all markers studied.
Conclusions: Prostate biopsies showed statistically significant differences in T-cell markers, particularly when we compared between the tumor-free region surrounding PC in black men against all 3 regions in white men. These data suggest black men have higher expression of T-cells surrounding PC regions, generating a pro-tumor inflammatory micro-environment, which may in part contribute to PC racial disparity.
Source of Funding: Supported by National Institutes of Health; Grant number: K24 CA160653, and Department of Defense Award: DOD W81XWH-16-1-0750. Adriana Vidal was supported by a Research Scholar Grant, RSG-18-018-01 - CPHPS, from the American Cancer Society. Andrew Bosomwo